Document Detail


Essentials of Th17 cell commitment and plasticity.
MedLine Citation:
PMID:  23325835     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
CD4(+) T helper (Th) cells exist in a variety of epigenetic states that determine their function, phenotype, and capacity for persistence. These polarization states include Th1, Th2, Th17, and Foxp3(+) T regulatory cells, as well as the more recently described T follicular helper, Th9, and Th22 cells. Th17 cells express the master transcriptional regulator retinoic acid-related orphan receptor γ thymus and produce canonical interleukin (IL)-17A and IL-17F cytokines. Th17 cells display a great degree of context-dependent plasticity, as they are capable of acquiring functional characteristics of Th1 cells. This late plasticity may contribute to the protection against microbes, plays a role in the development of autoimmunity, and is necessary for antitumor activity of Th17 cells in adoptive cell transfer therapy models. Moreover, plasticity of this subset is associated with higher in vivo survival and self-renewal capacity and less senescence than Th1 polarized cells, which have less plasticity and more phenotypic stability. New findings indicate that subset polarization of CD4(+) T cells not only induces characteristic patterns of surface markers and cytokine production but also has a maturational aspect that affects a cell's ability to survive, respond to secondary stimulation, and form long-term immune memory.
Authors:
Pawel Muranski; Nicholas P Restifo
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Intramural; Review     Date:  2013-01-16
Journal Detail:
Title:  Blood     Volume:  121     ISSN:  1528-0020     ISO Abbreviation:  Blood     Publication Date:  2013 Mar 
Date Detail:
Created Date:  2013-03-29     Completed Date:  2013-06-03     Revised Date:  2014-03-31    
Medline Journal Info:
Nlm Unique ID:  7603509     Medline TA:  Blood     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2402-14     Citation Subset:  AIM; IM    
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MeSH Terms
Descriptor/Qualifier:
Cell Differentiation / immunology*
Cell Polarity / immunology
Graft vs Host Disease / immunology
Humans
Immunity, Innate / immunology
Immunologic Memory / immunology*
Infection / immunology
Models, Biological
Neoplasms / immunology
Th17 Cells / immunology,  physiology*
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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